Presentation Title

Removal of Beta-Amyloid and Tau Proteins Lead to Death in Alzheimer's Patients

Start Date

November 2016

End Date

November 2016

Location

HUB 367

Type of Presentation

Oral Talk

Abstract

Alzheimer's disease is a type of progressive brain disorder caused by the presence of both neurofibirillary tangles and senile plaques. Plaque is made of beta-amyloid protein fragments and tangles are formed from tau proteins. The synapse, the main signaling connectors of the brain, is damaged through the clumps of protein leading to brain cell death. Although previous studies have shown antibody medication, aducanumab, eradicating the plaques it is unclear why many patients die after treatment. To address this issue, I am conducting a meta-analysis of scholarly journals and books that reveal the beta-amyloid protein peptide deposits are surrounded by tau-immureactive neurites that require a high concentration of antibody medication to be removed. While the deposits are not toxic by themselves, the over expression and stimulation of the plaques and tangles through the antibodies lead to mutations that result to behavioral deficits. This study shows that the removal of beta-amyloid and tau proteins from antibody medication is globally and persistently mutated after a noxious stimulus. Such a stimulus might serve to explain the side-effects from the arousal reaction from antibodies.

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Nov 12th, 2:30 PM Nov 12th, 2:45 PM

Removal of Beta-Amyloid and Tau Proteins Lead to Death in Alzheimer's Patients

HUB 367

Alzheimer's disease is a type of progressive brain disorder caused by the presence of both neurofibirillary tangles and senile plaques. Plaque is made of beta-amyloid protein fragments and tangles are formed from tau proteins. The synapse, the main signaling connectors of the brain, is damaged through the clumps of protein leading to brain cell death. Although previous studies have shown antibody medication, aducanumab, eradicating the plaques it is unclear why many patients die after treatment. To address this issue, I am conducting a meta-analysis of scholarly journals and books that reveal the beta-amyloid protein peptide deposits are surrounded by tau-immureactive neurites that require a high concentration of antibody medication to be removed. While the deposits are not toxic by themselves, the over expression and stimulation of the plaques and tangles through the antibodies lead to mutations that result to behavioral deficits. This study shows that the removal of beta-amyloid and tau proteins from antibody medication is globally and persistently mutated after a noxious stimulus. Such a stimulus might serve to explain the side-effects from the arousal reaction from antibodies.